Cardiovascular & Renal · Full case

Acute Kidney Injury

NICE CG169AKI Network StagingSTOP Nephrotoxics

AKI Stage 1: creatinine ×1.5 above baselineThe AKIN (Acute Kidney Injury Network) / KDIGO staging system defines AKI in three stages: Stage 1 — creatinine rises to 1.5–1.9× baseline (or rises ≥26µmol/L within 48 hours); or urine output <0.5ml/kg/hour for 6–12 hours. Stage 2 — creatinine rises to 2.0–2.9× baseline; or urine output <0.5ml/kg/hour for ≥12 hours. Stage 3 — creatinine rises to ≥3.0× baseline (or ≥354µmol/L with an acute rise of ≥26µmol/L); or initiation of renal replacement therapy; or urine output <0.3ml/kg/hour for ≥24 hours (anuria ≥12 hours). In primary care, “baseline creatinine” is the most recent creatinine within the past 3 months (or up to 12 months if no acute illness in that period). Without a baseline, any creatinine above the age-adjusted upper limit of normal should raise suspicion.

STOP nephrotoxics immediatelyThe immediate pharmacological intervention in any AKI: STOP NEPHROTOXIC DRUGS. The most important categories: (1) NSAIDs — constrict afferent arterioles; reduce GFR; can precipitate and perpetuate AKI. (2) ACE inhibitors and ARBs — dilate efferent arterioles; reduce GFR in low-renal-perfusion states (dehydration; sepsis; cardiac failure); must be held in AKI. (3) Metformin — accumulates in renal failure; risk of lactic acidosis; must be withheld when GFR is falling or uncertain. (4) Aminoglycosides (gentamicin; tobramycin): direct tubular toxicity; avoid or use with close monitoring. (5) Contrast agents (iodinated IV contrast): contrast-induced nephropathy — ensure hydration; consider N-acetylcysteine in high-risk cases. (6) Diuretics: can worsen prerenal AKI (volume depletion); withhold or use cautiously. The “sick day rules” (SADMAN) remind patients which drugs to stop when acutely unwell.

Hyperkalaemia >6.5 mmol/L = emergencyHyperkalaemia is the most immediately life-threatening complication of AKI. Potassium >6.5 mmol/L (or any level with ECG changes) = medical emergency requiring hospital admission for cardiac monitoring; IV calcium gluconate (membrane stabilisation); insulin/dextrose infusion; salbutamol nebuliser; sodium bicarbonate if acidotic; polystyrene sulphonate resin or patiromer (Veltassa) for short-term reduction; dialysis if severe. ECG changes in hyperkalaemia: tall peaked T waves (earliest sign); PR prolongation; widened QRS complex; sine wave pattern; ventricular fibrillation. Even K+ 5.5–6.5 mmol/L in AKI requires urgent review: stop K+-retaining drugs (ACEi; ARBs; potassium-sparing diuretics); dietary advice; emergency review if rising. NEVER give potassium chloride IV fluid in AKI without careful monitoring.

SADMAN sick-day rulesSADMAN is a mnemonic for the drugs patients should STOP when acutely unwell (vomiting; diarrhoea; sweating; reduced fluid intake; fever): S — Sulphonylureas (gliclazide; glipizide — hypoglycaemia risk with reduced intake); A — ACE inhibitors / ARBs (reduce GFR in dehydration); D — Diuretics (worsen volume depletion); M — Metformin (lactic acidosis risk if GFR falls); A — NSAIDS (nephrotoxic; constrict afferent arteriole); N — NOAC/newer anticoagulants (accumulate in renal failure; haemorrhage risk). These “sick-day rule” medications should be withheld if the patient is unwell, unable to maintain oral hydration, or has diarrhoea/vomiting, and should be restarted only once recovered (usually after 24–48 hours of normal eating and drinking). Providing written sick-day rule information reduces AKI incidence and severity in high-risk patient populations.

Pre-renal AKI: most common type in GP (70%)Pre-renal AKI (volume depletion; reduced renal perfusion) is the most common type encountered in primary care, accounting for approximately 70% of community-acquired AKI. Causes: dehydration (vomiting; diarrhoea; poor intake; heat exposure); blood loss; sepsis-related hypoperfusion; cardiac failure (reduced cardiac output); hepatorenal syndrome; excessive diuretic therapy; NSAIDs; ACEi/ARB in susceptible patients. Pre-renal AKI is rapidly reversible with appropriate fluid resuscitation and removal of precipitants. Key feature: high urine osmolality; concentrated urine; urine:plasma urea ratio >10:1; urine sodium <20 mmol/L (kidney is retaining sodium in response to low perfusion). If pre-renal AKI is not corrected, it progresses to intrinsic (ischaemic) AKI (acute tubular necrosis; ATN), which takes days–weeks to recover.

AKI recovery: re-introduce ACEi/ARBs at 4–6 weeksAfter AKI has resolved, medications held during the acute episode should be systematically reviewed before re-introduction. The most important decision: ACE inhibitors and ARBs. These drugs can be restarted once renal function has stabilised back to (or close to) baseline. The recommended approach (NICE CG169): do not routinely restart ACEi/ARBs until renal function has returned to baseline and the patient is clinically well; generally 4–6 weeks post-AKI; check eGFR and electrolytes before restarting; monitor eGFR and K+ 1–2 weeks after restarting. NSAIDs: do not restart in patients with CKD or those at high risk of AKI recurrence. Metformin: restart once eGFR >30 ml/min/1.73m² and patient is clinically well. Document all drug changes and the plan to review in the notes.

Urinary obstruction (post-renal): ultrasoundPost-renal AKI (obstructive) accounts for approximately 10% of AKI in the community, rising to higher proportions in elderly men (prostatic obstruction) and patients with gynaecological or retroperitoneal malignancy. The diagnosis must not be missed — obstruction is rapidly reversible if relieved early but causes irreversible tubular damage (obstructive uropathy) if chronic. Red flags for obstructive AKI: oliguria or anuria; palpable bladder (urinary retention); known or suspected malignancy (cervical; prostate; colorectal; retroperitoneal); history of BPH; previous stones; recent pelvic/abdominal surgery. Investigation: renal USS — first-line for diagnosing hydronephrosis (dilated pelvi-calyceal system); bladder scan. Management: bladder catheterisation for retention; urology referral if upper tract obstruction; nephrostomy if bilateral upper tract. Obstruction must be excluded in ALL patients presenting with AKI — particularly if anuria is present.

AKI: 1-year mortality 20–25%AKI is associated with significant short and long-term mortality. In-hospital AKI: 1-year mortality 20–25%; community-acquired AKI: approximately 10–20% 90-day mortality depending on severity and comorbidities. AKI is also a major risk factor for: progression to CKD (25–30% of patients who survive AKI develop incident or worsening CKD); cardiovascular events (AKI is an independent risk factor for MI; stroke; heart failure in the year following the episode); recurrent AKI; ESRD. GP role: ensure all patients who have had AKI receive a follow-up creatinine at 4–6 weeks; 3 months post-AKI; and at least annually thereafter. At each follow-up: check creatinine; eGFR; urine ACR (proteinuria — a marker of renal injury); blood pressure; medication review.

📋 Clinical Stem — Acute Kidney Injury

Mr. Derek Patel, 72, with type 2 diabetes; hypertension; and CKD stage 3a (eGFR baseline 52), presenting after 4 days of diarrhoea and vomiting, on metformin; lisinopril; ibuprofen (self-medicating); and furosemide, with a creatinine today of 218 µmol/L (baseline 105 µmol/L) and potassium 5.9 mmol/L

Mr. Derek Patel, 72, a retired engineer with type 2 diabetes; hypertension; and established CKD stage 3a (last eGFR 52; creatinine 105 µmol/L six weeks ago), presents to the GP surgery after 4 days of diarrhoea and vomiting. His wife called this morning because he is lethargic; oliguric; and “not himself.” He is on: metformin 1g BD; lisinopril 5mg OD; furosemide 40mg OD; amlodipine 5mg OD; atorvastatin 40mg OD. He has been self-medicating with ibuprofen 400mg TDS for 4 days (bought from a supermarket) for back pain. His blood test results today: creatinine 218 µmol/L; potassium 5.9 mmol/L; sodium 133 mmol/L; urea 18.4 mmol/L; eGFR 23; CRP 42; WCC 11.2; Hb 131 g/L. BP 98/62; HR 108; temp 37.8°C; RR 20.

This stem tests: AKI recognition and staging (Stage 2: creatinine 218 vs baseline 105 = 2.08× baseline); identification of multiple precipitants (ibuprofen; lisinopril; furosemide; dehydration from D&V); SADMAN medication management (STOP metformin; lisinopril; furosemide; ibuprofen immediately); hyperkalaemia management (K+ 5.9 = urgent; not yet emergency but requires immediate action); fluid assessment (dehydrated: tachycardia; hypotension; low Na); decision to admit vs manage in community; and the sick-day rules education that should follow recovery.

Scenario A — Mr. Patel (AKI Stage 2; multiple precipitants; K+ 5.9) Creatinine 218 (baseline 105) = 2.08× = Stage 2. K+ 5.9 = urgent. Dehydrated + hypotensive. On ibuprofen; lisinopril; furosemide; metformin. STOP all four immediately. Admit for IV fluids; cardiac monitoring; electrolyte management. This is a hospital admission — cannot manage community. SADMAN education post-recovery. ACEi restart at 4–6 weeks once eGFR recovered.

Scenario B — Mild AKI Stage 1; community management Creatinine 142 (baseline 95) = 1.49× = Stage 1. Potassium 5.2. Clinically well; normotensive; taking oral fluids. Pre-renal cause (D&V 2 days). STOP NSAIDs; ACEi; diuretics; metformin. Encourage oral fluid intake. Repeat bloods in 24–48 hours. Clear criteria for escalation (worsening; oliguric; K+ rising; unable to drink). Sick-day rules education. Do not admit if Stage 1 and clinically stable.

Scenario C — AKI with hyperkalaemia >6.5 mmol/L K+ 6.8 mmol/L. EMERGENCY. 999. IV calcium gluconate (membrane stabilisation); insulin/dextrose; salbutamol nebuliser. ECG immediately: peaked T waves; widened QRS. Stop all K+-retaining drugs. Hospital admission mandatory. Consider dialysis if K+ rising despite treatment or anuric.

Scenario D — AKI with suspected obstruction Elderly man; BPH history; anuric; palpable bladder. Post-renal AKI (obstruction). Bladder scan first. Catheterise urgently (urinary retention). Urology referral. Renal USS to check for hydronephrosis. Creatinine may fall rapidly after decompression — “post-obstructive diuresis” (may need IV fluid replacement).

Scenario E — Post-AKI follow-up (recovery monitoring) Patient recovering at home after hospital admission for AKI. GP follow-up: creatinine at 4–6 weeks (has it returned to baseline?); medication review (when to restart ACEi; ARBs; metformin); urine ACR (proteinuria post-AKI); BP; eGFR trajectory. SADMAN education. CKD coding if eGFR remains below baseline. Annual renal function monitoring thereafter.

Key variables to adapt for AKI stage (1 vs 2 vs 3 — determines admit vs community); K+ level (5.5–6.5 = urgent; >6.5 = emergency); fluid status (dehydrated vs fluid overloaded — cardiac failure AKI requires a different approach); precipitant (pre-renal vs intrinsic vs post-renal); medication burden (SADMAN drugs present); baseline CKD (higher risk of AKI and slower recovery); AKI in context of sepsis (source must be identified and treated); obstruction features (anuria; retention; malignancy)

Steps:

Step 1

History — Precipitant · Duration · Urine Output · SADMAN Drugs · Fluid Balance

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AKI history has one primary objective: identify the precipitant and assess severity so the immediate management decisions — STOP nephrotoxics; admit vs community; IV fluids vs oral — can be made urgently. Mr. Patel has four simultaneous precipitants: NSAID (ibuprofen); ACEi (lisinopril); diuretic (furosemide); and volume depletion from D&V. Identifying all four is essential — failing to stop any one perpetuates the AKI.

🎓 SCA opener — AKI is urgent; the opener must establish the clinical picture rapidly while acknowledging concern

"Mr. Patel; I can see from your blood tests that your kidneys are under significant stress — I want to understand what has been happening over the last few days. Can you tell me about the diarrhoea and vomiting — when it started; how much you have been able to drink; and whether your urine has changed?"

AKI is a time-critical condition. The SCA opener acknowledges what the blood tests show (clinical context already established) and immediately directs to the three most urgent history items: precipitant duration; fluid intake; and urine output. This is not a situation for a purely open, leisurely history — a structured urgent approach is appropriate and will be recognised as such.

1A — Targeted AKI history

Question	Why it matters	Changes what?
🏲 FOCUSED OPENER"Tell me about the diarrhoea and vomiting — when did it start; how often; are you still being sick? And crucially — how much have you been able to drink in the last 24 hours?"	Duration and severity of fluid losses establish whether this is predominantly pre-renal (most likely in Mr. Patel) and how severe the volume depletion is. 4 days of D&V with reduced oral intake = significant volume depletion. This, combined with lisinopril (efferent dilation; reduces GFR), furosemide (further volume depletion), and ibuprofen (afferent constriction; reduces GFR), creates a “perfect storm” for AKI. Each precipitant must be identified independently — removing one without the others may be insufficient.SCA: Tasks — identifying ALL precipitants drives the STOP nephrotoxics decision	Pre-renal confirmed; multiple precipitants; volume depletion severity; hospital admission decision
Urine output history"How much urine have you been passing? Has it been much less than normal? Any change in colour?"	Oliguria (<0.5 ml/kg/hour; <approximately 30 ml/hour for an average adult) is both a diagnostic criterion for AKI and a marker of severity. Mr. Patel’s wife noted he “is not himself” — oliguria combined with lethargy is a concerning combination. Complete anuria (<100 ml/24 hours): consider obstruction (do not assume all AKI is pre-renal — obstruction must be excluded). Dark concentrated urine: suggests pre-renal. Haematuria: consider intrinsic renal disease; glomerulonephritis; obstructive stone; or transitional cell carcinoma if painless.	Oliguria: AKI confirmed; severity staging. Anuria: obstruction must be excluded immediately (bladder scan; catheter). Haematuria: glomerulonephritis; stone; malignancy — specialist urgent referral
Complete medication history — SADMAN"Tell me all the tablets you take. Have you taken any painkillers recently — including ones you bought yourself?"	Mr. Patel has not volunteered the ibuprofen — the GP must specifically ask about OTC medications. The SADMAN drugs in Mr. Patel: S (sulphonylurea — no; on metformin); A (ACEi: lisinopril — must stop); D (diuretic: furosemide — must stop); M (metformin — must stop; lactic acidosis risk); A (NSAID: ibuprofen — must stop; major precipitant); N (NOAC — not on one). Without asking about OTC medications, the ibuprofen — which is a major precipitant — will not be identified. Ibuprofen + lisinopril + furosemide + dehydration = “triple whammy” combination: one of the most dangerous polypharmacy combinations for AKI.	Ibuprofen: STOP immediately; precipitant. Lisinopril: STOP. Furosemide: STOP. Metformin: STOP (lactic acidosis). All four actions must be taken at this consultation. Restart plan documented.
Infection source — sepsis assessment"Do you have any other symptoms — fever; urinary symptoms; cough; rigors? Has your back been painful — and if so, is it a new kind of pain?"	Sepsis is both a cause and a complication of AKI. Mr. Patel: CRP 42; WCC 11.2; temp 37.8°C; HR 108 — a systemic inflammatory response pattern. Source: the D&V may indicate gastrointestinal infection; the back pain may indicate pyelonephritis. Pyelonephritis in a diabetic with CKD — this is a serious combination and one that requires IV antibiotics. The qSOFA score (RR ≥22; GCS <15; SBP ≤100mmHg): SBP 98 = positive; RR 20 = borderline. The NEWS2 or qSOFA should be calculated in any patient with suspected sepsis in the community.	Sepsis screen: SEPSIS 6 (blood cultures; broad-spectrum antibiotic; IV fluid; O2; urine output monitoring; lactate). qSOFA ≥2: urgent hospital transfer. Source identification drives antibiotic choice.
Baseline renal function and risk factors"What were your kidneys like before this? I know you have CKD — what eGFR were you running at? Any diabetes complications; heart failure; liver disease?"	Baseline CKD Stage 3a (eGFR 52; creatinine 105) is critical context. Creatinine today: 218 = 2.08× baseline = AKI Stage 2. Without the baseline, AKI staging is impossible. Pre-existing CKD dramatically amplifies AKI risk (less renal reserve) and slows recovery. Other risk factors that worsen AKI prognosis: diabetes (renal microvascular disease; autonomic neuropathy affects urine sensation); heart failure (low perfusion); liver disease (hepatorenal syndrome); older age; multiple nephrotoxins.	AKI Stage 2 (2.08× baseline). CKD baseline: expect slower recovery; closer monitoring. Hospital admission more likely with CKD background + Stage 2 + K+ 5.9.
Obstruction screen"How has the urine been? Any difficulty passing it? Any sense that you can’t empty your bladder fully? Any urinary symptoms before this — poor stream; nocturia?"	Post-renal obstruction must always be excluded in AKI, particularly in elderly men (prostatic obstruction is common). If Mr. Patel has anuria rather than oliguria: obstruction is more likely and a bladder scan is urgent. His back pain could represent ureteric obstruction (calculus; extrinsic compression) in addition to the pre-renal picture. Red flags for post-renal AKI: palpable bladder; history of BPH; acute urinary retention; malignancy; loin-to-groin pain (stone). If in doubt: catheterise and measure residual volume.	Post-renal suspected: bladder scan; catheterisation; renal USS (hydronephrosis); urology referral. BPH + oliguria: catheterise first; monitor urine output after.

1B — Red flags — immediate action required

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Red Flags — requiring 999 / same-day hospital admission

Red flag	Why dangerous	Action
K+ >6.5 mmol/L or any K+ with ECG changes	Hyperkalaemia causes fatal cardiac arrhythmia. ECG changes (peaked T waves; widened QRS; sine wave) indicate imminent ventricular fibrillation. Requires IV calcium gluconate (membrane stabilisation); insulin/dextrose; salbutamol; dialysis if unresponsive. Cannot manage in primary care without IV access and cardiac monitoring.	999 — hospital resuscitation; IV calcium gluconate immediately; ECG
qSOFA ≥2 (SBP ≤100; RR ≥22; GCS <15)	Sepsis with organ dysfunction (septic shock). Mr. Patel: SBP 98 = 1 point; RR 20 (borderline). Any two = sepsis emergency. Sepsis + AKI = septic AKI. Sepsis 6 (blood cultures; IV antibiotics; IV fluids; O2; monitoring; lactate) must be initiated within the hour. Cannot be managed in primary care.	999 — Sepsis 6 pathway; IV antibiotics within 1 hour
Anuria (<100 ml/24 hours)	Complete anuria (not oliguria) strongly suggests obstruction (retention) or severe intrinsic AKI (bilateral renal artery disease; vasculitis; rapidly progressive glomerulonephritis). Must exclude obstructive cause immediately: bladder scan; catheterise. Anuria with rising creatinine = same-day urology or nephrology.	Same-day hospital; bladder scan; catheterise; nephrology / urology; renal USS
AKI Stage 3 (creatinine ≥3× baseline or ≥354 µmol/L)	Severe renal failure. Risk of pulmonary oedema; metabolic acidosis; uraemic encephalopathy; haemorrhage; cardiac arrest. Almost always requires hospital admission; likely nephrology involvement; may require RRT (renal replacement therapy / dialysis).	Same-day hospital; nephrology urgent referral; prepare for RRT
Pulmonary oedema; severe metabolic acidosis (pH <7.2); uraemic encephalopathy	AKI complications: fluid overload causing pulmonary oedema (particularly if oliguric); severe metabolic acidosis (unmeasured anion gap in AKI from retained H+); uraemic encephalopathy (encephalopathy; asterixis; seizures; coma from retained uraemic toxins). All require immediate hospital; likely ICU or HDU.	999 — ICU/HDU; dialysis likely

🛡️

Safeguarding — AKI in Older Adults and Polypharmacy

Mr. Patel is 72; has CKD; diabetes; and was self-medicating with ibuprofen. AKI in older adults with multimorbidity is a preventable patient safety event. The ibuprofen was bought OTC without awareness of the contraindication. SADMAN education at every NSAID prescription and at every chronic disease review is a preventive safeguarding measure.

💊 Medication safety

NSAIDs are contraindicated in CKD (eGFR <60) and should not be sold OTC to patients on ACEi + diuretics — document the “triple whammy” risk in every diabetes/CKD review
SADMAN written information must be provided to ALL patients on ACEi; ARBs; diuretics; metformin; NSAIDs — document provision in notes
Metformin: must carry current maximum eGFR threshold warning (stop if eGFR <30; reduce dose 30–45)

🧑️ Capacity and carer involvement

Mr. Patel’s wife called this morning — she is his carer and informant. Include her in the management discussion (with consent)
If patient is confused or encephalopathic: assess capacity; MCA 2005 applies; next-of-kin / carer decision-making if lacking capacity
Document Glasgow Coma Scale or AVPU at this consultation — altered consciousness in AKI is an emergency indicator

🚘 Community vs hospital decision

AKI Stage 2 with K+ 5.9; hypotension (SBP 98); and CKD background in a 72-year-old = hospital admission. Never compromise on admission criteria for patient preference alone
If patient declines admission: document clearly; capacity assessment; involve next-of-kin; establish safety-netting; arrange same-day GP review; 999 criteria explained

📸 Sick-day rules education

This AKI was preventable — SADMAN education should have prevented the ibuprofen use
At every CKD review; diabetic check; and blood pressure review: provide SADMAN written information
On discharge post-AKI: written SADMAN guide must be provided; document in notes

Actions: NEWS2 / qSOFA calculated and documented; SADMAN medications identified (all four: ibuprofen; lisinopril; furosemide; metformin); hospital admission arranged (AKI Stage 2 + K+ 5.9 + haemodynamically compromised); carer involved; medication changes clearly documented.

1C — PMH · Drug history · Social history

🥐 PMH · Risk factors for AKI

Factor	Why it matters	Impact
CKD Stage 3a (baseline eGFR 52)	CKD dramatically increases AKI risk (reduced renal reserve) and slows recovery. Patients with CKD Stage 3 have a 3–5× higher AKI risk than those with normal renal function. CKD also means AKI staging is possible (known baseline creatinine: 105 µmol/L). Post-AKI: eGFR may not return to pre-AKI baseline in CKD — plan for monitoring and potential CKD stage upgrade.	AKI Stage 2 confirmed (creatinine 218 = 2.08× baseline 105). Slower recovery expected. Post-AKI creatinine may not return to 105; monitor at 4–6 weeks; 3 months; annually
Type 2 Diabetes	Diabetic nephropathy is the most common cause of CKD in the UK. Autonomic neuropathy may reduce sensation of oliguria. Diabetic patients have higher risk of AKI from contrast; sepsis; and nephrotoxins. Metformin (in Mr. Patel) requires specific management in AKI: risk of lactic acidosis if eGFR falls — MUST be stopped immediately when AKI is suspected.	Metformin: STOP immediately. Sulphonylurea: if present, monitor glucose (hypoglycaemia risk with reduced intake). Insulin management in hospital

🔴 The “Triple Whammy” in Mr. Patel

Drug	Mechanism of AKI	Action
Ibuprofen (OTC; self-medicating)	NSAIDs inhibit prostaglandin synthesis → afferent arteriolar constriction → reduced renal blood flow → GFR falls. In a dehydrated patient: prostaglandins are the main mechanism maintaining GFR — blocking them is catastrophic. Ibuprofen + ACEi + diuretic + dehydration = “triple whammy” (classically: NSAID + ACEi/ARB + diuretic) = extremely high-risk AKI combination. Contraindicated in CKD (eGFR <60) and in combination with ACEi.	STOP immediately. Do not restart. Contraindicated in CKD. Analgesia alternatives: paracetamol; codeine; tramadol with caution; specialist pain review
Lisinopril (ACEi)	ACE inhibitors dilate the efferent arteriole → reduce glomerular hydrostatic pressure → GFR falls in states of low renal perfusion (dehydration; haemodynamic compromise). Essential to stop in AKI but remember: ACEi provides renal protection in the long term (reduces proteinuria; slows CKD progression) — restart once recovered.	STOP immediately. Restart at 4–6 weeks post-AKI once eGFR returned to baseline. Check K+ and creatinine 1–2 weeks after restarting
Furosemide (loop diuretic)	Loop diuretic → natriuresis → volume depletion → pre-renal AKI. In a patient already dehydrated from D&V, furosemide accelerates the volume depletion and worsens pre-renal AKI. Also: hypokalaemia risk usually (but in this AKI with reduced GFR, potassium may actually accumulate — K+ is already 5.9 suggesting renal potassium retention is a larger problem).	STOP immediately. Restart once haemodynamically stable and eGFR recovering. Dose adjustment and monitoring after reintroduction
Metformin	Metformin is renally excreted. In AKI: metformin accumulates → impairs mitochondrial oxidative phosphorylation → lactic acidosis (life-threatening). Metformin should be stopped if eGFR <30; and withheld in any acute illness with AKI risk. Restart when eGFR >30 and patient is clinically well; eating and drinking normally.	STOP immediately. Restart when eGFR >30 and patient recovered. Monitor blood glucose during AKI (may need insulin; sliding scale if hospitalised)

1D — ICE

💡 Ideas

"Mr. Patel; do you understand what the blood test results mean? What do you think has happened to your kidneys?"

Mr. Patel may think his back pain (which prompted the ibuprofen use) is the main problem, and may not understand that the ibuprofen has contributed significantly to AKI. Many patients — particularly those with chronic conditions — have been told “avoid NSAIDs” but do not understand the mechanism or the severity of the risk. The illness model conversation is also an opportunity to explain the “triple whammy” in simple terms: “Your kidneys were already working harder than usual with the CKD. The diarrhoea and vomiting dried you out. The ibuprofen — which is a strong painkiller — reduced the blood supply to your kidneys. And the blood pressure tablet and the water tablet also slowed things down when you are dry. All four together hit your kidneys at once.”

😟 Concerns

"What worries you most about what is happening? Are you worried about whether your kidneys will recover? About going to hospital?"

Patients with CKD fear progression to dialysis. The reassurance must be specific and honest: “AKI from the causes you have — dehydration and the medications — usually recovers well with the right treatment. We are catching this at a stage where treatment will make a significant difference. I cannot guarantee your kidneys will return to exactly where they were — but the likely outcome with prompt treatment is good.” Acknowledge the hospital concern: explain why admission is necessary and what will happen.

🎯 Expectations

"What did you think we would do today? Were you hoping to stay at home, or were you aware this might need hospital treatment?"

Mr. Patel may be expecting reassurance and a prescription change. The expectation of hospital admission must be managed carefully — it is the correct clinical decision and must not be compromised by patient preference alone. The explanation must be clear: “I need to be honest with you — with the blood test results showing your kidney function has significantly dropped AND your potassium is elevated — you need to be in hospital where they can give you IV fluids and monitor your heart. This is not something I can safely manage at home today.”

🎓 SCA Checkpoint — Step 1TasksGlobal Skills

Key SCA phrases

"Mr. Patel — I need to ask specifically: have you taken any painkillers in the last week, including anything you bought from a pharmacy or supermarket?"

"I want to make sure I understand everything you are taking — because some tablets are fine normally but can be harmful to the kidneys when you are dehydrated like this. The ibuprofen you have taken — that is one of the main things that has put your kidneys under stress."

Deductions

Not asking specifically about OTC medications — the ibuprofen is the major identifiable precipitant; missing it means an incomplete SADMAN assessment
Not asking about urine output — oliguria is both a diagnostic criterion and an admission criterion

🔴 Red

Ibuprofen not identified; SADMAN drugs not stopped; K+ 5.9 not acted upon; hospital admission not arranged; urine output not assessed; no sepsis assessment; obstruction not excluded

🟠 Amber

Ibuprofen identified; lisinopril stopped; hospital admission arranged; K+ 5.9 recognised as urgent; furosemide and metformin not stopped; SADMAN not fully explained; sick-day rules education not given; ACEi restart plan not documented

🟩 Green

All four SADMAN drugs identified and stopped (ibuprofen; lisinopril; furosemide; metformin); K+ 5.9 urgent — hospital admission; AKI Stage 2 staged correctly; sepsis features assessed (qSOFA); obstruction excluded; hospital arranged with 999 if haemodynamic instability; SADMAN education and written information; ACEi restart plan (4–6 weeks post-recovery); 4–6 week blood test follow-up; closing question

Step 2

Triage — AKI Emergency · Urgent Admission · Community-Manageable Stage 1

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Mr. Patel requires hospital admission: AKI Stage 2 + K+ 5.9 + haemodynamic compromise (SBP 98; HR 108) + sepsis features + background CKD + metformin risk. This is not a community-manageable AKI. The triage decision is essentially: 999 now vs urgent (same-day) hospital transfer.

🔴 Emergency — 999

Immediate Life-Threatening

999 now

K+ >6.5 mmol/L or ECG changesIV calcium gluconate; insulin/dextrose; 999
qSOFA ≥2 (septic shock)Sepsis 6; 999; IV antibiotics within 1 hour
AKI Stage 3; anuria; pulmonary oedema; encephalopathy999; ICU/HDU; dialysis likely

🟠 Urgent — Mr. Patel

Same-Day Hospital (Not 999 Yet)

Emergency referral

AKI Stage 2 + K+ 5.9 + haemodynamic compromise + CKD backgroundCall medical registrar; transfer by ambulance; STOP SADMAN drugs now
AKI + sepsis features + CRP/WCC elevatedSepsis work-up in hospital; blood cultures; IV antibiotics

🟩 Community-manageable

AKI Stage 1; Clinically Well

Close GP monitoring

Stage 1; normotensive; drinking; K+ <5.5STOP SADMAN; increase oral fluids; repeat bloods 24–48h; escalation criteria given
Clear pre-renal cause; no systemic features; improvingCommunity management safe; arrange same-day if worsening

🎓 SCA Checkpoint — Step 2TasksGlobal Skills

Hospital admission conversation — non-negotiable

"Mr. Patel — I need to be direct with you. Your blood tests show that your kidneys are working at about half the level they were six weeks ago. Your potassium level is elevated — which can affect your heart. And your blood pressure is lower than it should be. All of this together means I need to arrange for you to go to hospital today, where they can give you fluids directly into your veins and monitor your heart closely. I know that is not what you were hoping to hear — but this is not something I can safely manage at home."

Deductions

Not arranging hospital admission for AKI Stage 2 + K+ 5.9 + haemodynamic compromise — this is a patient safety failure; community management is inappropriate and potentially fatal

Step 3

Examination — Fluid Status · Haemodynamics · Obstruction Screen · Sepsis Signs

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AKI examination has four priorities: (1) fluid status (dehydration vs fluid overload); (2) haemodynamic stability (determines urgency); (3) obstruction signs (palpable bladder; loin tenderness); (4) infection source (sepsis).

Examination	What it shows	Management impact	Changes?
Fluid statusSkin turgor; mucous membranes; JVP; capillary refill; postural BP; peripheral oedema	The most critical examination in pre-renal AKI. Dehydration signs (Mr. Patel): dry mucous membranes; reduced skin turgor; sunken eyes; postural hypotension; tachycardia; low JVP; prolonged capillary refill. These confirm the pre-renal picture. Conversely: elevated JVP; bibasal crackles; peripheral oedema — suggests fluid overload AKI (cardiac failure; nephrotic syndrome) where IV fluids would be HARMFUL — a fundamentally different management pathway requiring diuresis (specialist-guided) not fluid resuscitation.	Dehydrated: IV 0.9% NaCl resuscitation in hospital. Fluid overloaded: IV diuretics (specialist); fluid resuscitation harmful. Equivocal: admit for monitoring	YES — fundamental management fork: IV fluids vs withhold fluids
Haemodynamics — BP; HR; RR; temp; O2 satNEWS2 or qSOFA calculation	Mr. Patel: BP 98/62; HR 108; RR 20; temp 37.8°C. qSOFA: SBP ≤100 (1 point); RR ≥22 (borderline; 20 = 0 points); GCS <15 (if confused = 1 point). NEWS2: BP 98 → high score. These haemodynamic parameters are the key triage determinants — SBP <90 requires 999; SBP 90–100 with other features: urgent same-day hospital transfer. Document NEWS2 or qSOFA in the notes as this is medicolegally important.	SBP <90: 999 ambulance. SBP 90–100 with other AKI features: urgent hospital transfer by ambulance. If haemodynamically stable Stage 1: community monitoring possible	YES — haemodynamics determine 999 vs urgent vs community management
Bladder palpation; loin examinationSuprapubic fullness; bimanual palpation; loin tenderness; renal angle percussion	Palpable bladder: urinary retention (post-renal obstruction). Loin pain and tenderness: pyelonephritis (infection source; particularly relevant in diabetic with D&V and elevated CRP); renal calculus; upper tract obstruction. Mr. Patel: if he has loin tenderness — pyelonephritis must be considered as the sepsis source. If bladder palpable: catheterise immediately to decompress and measure urine output.	Palpable bladder: catheterise; post-renal AKI. Loin tenderness: pyelonephritis — urine culture; IV antibiotics in hospital. Renal angle percussion positive: calculus or obstruction; USS urgently	YES — determines post-renal (obstruction) vs intrinsic (infection) cause
Neurological assessment; GCSLevel of consciousness; asterixis (metabolic flap); drowsiness	Uraemic encephalopathy: confusion; drowsiness; asterixis (flapping tremor — ask patient to hold hands outstretched; a flapping tremor indicates metabolic encephalopathy from uraemia; hepatic failure; or severe hypercapnia). Confusion in AKI + hyperkalaemia = extreme urgency. Mr. Patel: wife says he is “not himself” — baseline mental status must be established and documented. Any change from baseline = clinical red flag driving more urgent action.	Confusion or GCS <15: 999; ICU/HDU consideration. Asterixis: uraemic encephalopathy; urgent dialysis assessment	YES — encephalopathy = 999; ICU pathway; dialysis assessment

🎓 SCA Checkpoint — Step 3Tasks

Examination communication

"Mr. Patel, I want to check a few things — your blood pressure; heart rate; and I want to feel your tummy and check whether there is any fluid collecting or any tenderness over your kidneys. I also want to ask — are you feeling confused at all, or is your mind clear today?"

Deductions

Not assessing fluid status — the dehydrated vs fluid-overloaded distinction is the most fundamental examination decision in AKI; missing it means the wrong fluid management may be applied

Step 4

Investigations — Bloods · ECG (K+ >5.5) · Urine Dip/MSU · Bladder Scan · AKI Staging

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Blood tests are already back (done this morning). The key immediate investigation is ECG — K+ 5.9 mmol/L requires cardiac monitoring. Urine dipstick and MSU identify intrinsic renal disease or infection. Bladder scan excludes obstruction.

Investigation	When and why	Result and action
ECG — mandatory if K+ >5.5 mmol/LMr. Patel: K+ 5.9 — ECG must be performed NOW	Hyperkalaemia is the most immediately life-threatening AKI complication. K+ 5.9 mmol/L requires ECG to identify early cardiac changes. Changes in order of worsening hyperkalaemia: (1) Tall; peaked (tented) T waves (earliest sign — narrow-based; asymmetric; often in V1–V4); (2) PR prolongation (>200ms); (3) P wave flattening and disappearance; (4) QRS widening (>120ms); (5) Sine wave pattern (severe); (6) Ventricular fibrillation / asystole. ANY ECG change + K+ 5.9 = 999 immediately (IV calcium gluconate in ambulance). No ECG changes: still requires urgent hospital for monitoring — K+ can rise further quickly.	No ECG changes: urgent hospital (K+ 5.9 + AKI). ECG changes (peaked T; PR prolongation; QRS wide): 999 immediately; IV calcium gluconate. Sine wave / VF: CPR; 999.
Urine dipstick and MSUHaematuria; proteinuria; leucocytes; nitrites; casts	Urine dipstick in AKI: proteinuria (pre-existing CKD; nephrotic syndrome; intrinsic glomerular disease — particularly if heavy 3–4+ proteinuria); haematuria (glomerulonephritis; IgA nephropathy; vasculitis; stone; malignancy); leucocytes + nitrites (UTI; pyelonephritis — relevant in Mr. Patel with elevated CRP/WCC and loin pain). Urine microscopy: red cell casts = active glomerulonephritis (emergency nephrology); granular casts = acute tubular necrosis; white cell casts = pyelonephritis. MSU for MC&S: identify pyelonephritis organism; guide antibiotic choice.	Leucocytes + nitrites + pain: pyelonephritis — MSU; IV antibiotics in hospital. Haematuria + proteinuria (no infection): glomerulonephritis — urgent nephrology. Red cell casts: emergency nephrology. Isolated proteinuria: CKD; nephrology referral
Bladder scan — if anuria; retention suspectedPost-void residual >200 ml = significant retention	Bladder scan quantifies post-void residual urine volume — identifies urinary retention (post-renal obstruction). Not available in most GP surgeries — arrange urgently (district nurse; A&E; community nursing). If not available and retention is suspected: catheterise (if competent) or transfer urgently for catheterisation. Post-void residual >200 ml = significant retention; >400 ml = urgent catheterisation. Mr. Patel: oliguria but not anuria — retention less likely but should be considered if output does not improve with IV fluids in hospital.	Residual >200 ml: catheterise; post-renal AKI. Watch for post-obstructive diuresis (may need IV fluid replacement). Urology referral if upper tract obstruction (hydronephrosis on USS).
Renal USS — if obstruction or atypical AKIHydronephrosis; bladder size; echogenicity (CKD)	Renal USS is indicated in all patients with AKI if: (1) obstruction is suspected; (2) AKI cause is unclear after initial assessment; (3) no recovery after 24–48 hours of treatment; (4) recurrent AKI; (5) known urological malignancy. Renal USS findings: hydronephrosis (dilated pelvi-calyceal system = obstruction); small; echogenic kidneys (CKD — established chronic disease not acutely causing the AKI); normal appearances (pre-renal most likely if clinical picture fits). Not available immediately in primary care — arranged by medical team in hospital.	Hydronephrosis: obstruction; urology/nephrostomy. Normal: pre-renal or ATN. Small echogenic: underlying CKD (not obstructive). Mr. Patel: hospital team will arrange if not recovering with IV fluids.

🎓 SCA Checkpoint — Step 4Tasks

ECG and investigations

"Mr. Patel — your potassium level is raised. When potassium is high, it can affect your heart rhythm. I want to do an ECG — that is a tracing of your heart — right now to check that there are no changes. I also want to check your urine."

Deductions

Not performing ECG with K+ 5.9 mmol/L — peaked T waves from hyperkalaemia indicate imminent VF; missing this ECG is a patient safety failure

Step 5

Diagnosis — AKI Stage 2 · Pre-Renal · Plain Language · “Triple Whammy” Explained

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The diagnosis communication in AKI must explain the mechanism (pre-renal; multiple simultaneous precipitants); the severity (Stage 2; one step from severe); and why hospital admission is necessary — all without alarming the patient unnecessarily.

🗣️ Explaining AKI — the “triple whammy” in plain language

"Mr. Patel — I can see from your blood tests that your kidneys have been struggling over the last few days. Your kidney function has dropped to about half of where it was six weeks ago. Let me explain what has happened. Your kidneys already work a little harder than average because of your diabetes and CKD — they have less reserve. When you got the diarrhoea and vomiting, your body lost a lot of fluid. Normally your kidneys can cope with that, but you were also taking an ibuprofen tablet for your back pain — and ibuprofen reduces the blood flow to the kidneys, which is particularly dangerous when you are dry. On top of that, your blood pressure tablet — lisinopril — and your water tablet — furosemide — both also reduce kidney function when you are dehydrated. So all four things hit at once: the diarrhoea and vomiting; the ibuprofen; the blood pressure tablet; and the water tablet. That is why your kidneys are struggling — it is not one big single thing; it is four smaller things all at once. The good news is: this kind of kidney injury responds well to treatment, which is why I need to get you into hospital today where they can give you fluid through a drip and sort out your potassium level."

💬 Addressing specific concerns

"Will my kidneys recover? Will I need dialysis?"
"The honest answer is: we expect your kidneys to recover well because we have found this early and the cause is treatable — stopping the ibuprofen and rehydrating you will allow your kidneys to recover. I cannot promise they will return to exactly where they were before — but in most people with this type of kidney injury, the function does come back significantly. Dialysis is for very severe or prolonged kidney injury — that is not where you are right now, and that is not the expectation at this stage."

"Why do I need to go to hospital? Can you not give me fluids here?"
"I understand you would rather stay at home. But I have two specific concerns that need hospital management: first, your potassium level is elevated — when that happens, it can affect your heart rhythm, and I need you to be monitored. Second, you need fluids through a drip — drinking fluids alone is not fast enough when your kidneys are struggling this much. The hospital can correct both of those things safely, and that is what is going to get your kidneys better."

Mr. Patel’s Diagnosis

Hospital admission today

AKI Stage 2 (creatinine 218 vs baseline 105 = 2.08×). Pre-renal (volume depletion from D&V). Multiple precipitants: ibuprofen (OTC NSAID); lisinopril (ACEi); furosemide (diuretic); dehydration. Background CKD Stage 3a; T2DM; hypertension. K+ 5.9 mmol/L (urgent). Haemodynamic compromise (SBP 98; HR 108). Possible sepsis (CRP 42; WCC 11.2; temp 37.8). SADMAN drugs stopped. ECG performed. Hospital admission arranged.

Differential — Distinguish

Intrinsic AKI (ATN; GN)

Acute tubular necrosis (ATN): from ischaemia (prolonged pre-renal) or nephrotoxin. In Mr. Patel: if pre-renal not adequately treated, ATN supervenes. Signs: urine sodium >40; urine osmolality near plasma. Glomerulonephritis: haematuria + red cell casts; proteinuria; systemic features (rash; arthritis). Nephrology emergency.

Pyelonephritis-precipitated AKI

CRP 42; WCC 11.2; loin tenderness; diabetic = pyelonephritis must be excluded as the precipitant/contributor. MSU essential. IV antibiotics in hospital if confirmed.

AKI Staging (KDIGO)

Stage	Creatinine criteria	Urine output
Stage 1	1.5–1.9× baseline or rise ≥26 µmol/L in 48h	<0.5ml/kg/h for 6–12h
Stage 2 — Mr. Patel (2.08×)	2.0–2.9× baseline	<0.5ml/kg/h for ≥12h
Stage 3	≥3.0× baseline or ≥354 µmol/L or RRT	<0.3ml/kg/h for 24h or anuria 12h

🎓 SCA Checkpoint — Step 5TasksRelating to Others

AKI explanation — the triple whammy

"Four things happened at once. Your body lost fluid from the diarrhoea and vomiting. The ibuprofen you took reduced the blood flow to your kidneys — which is exactly what you cannot afford when you are dry. Your blood pressure tablet and your water tablet both slow the kidneys down further when you are dehydrated. All four hit together. Your kidneys were already working harder than average — so they had less room to cope."

Deductions

Attributing the AKI to only one cause (e.g. dehydration alone) without identifying the drug precipitants — the ibuprofen is the most preventable cause and the most important for future education

Step 6

Referral — Hospital Admission · Nephrology · Urology · AKI Network Alert

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Mr. Patel requires same-day hospital admission. The referral must communicate: AKI Stage 2; all precipitants (including ibuprofen — often missed); K+ 5.9; haemodynamic state; background CKD; SADMAN drugs already stopped.

Referral	Urgency	GP actions before transfer	What to communicate
Medical admission — Mr. Patel	Same-day — ambulance; not self-drive; haemodynamically compromised	STOP all four SADMAN drugs NOW (document in notes before transfer). ECG — perform and send with patient. Urine dip — MSU for MC&S before transfer if possible. IV access: if competent and equipment available; gain IV access before transfer (first line IV 0.9% NaCl could start). Copy of bloods for referring doctor. AKI alert: some labs generate automatic AKI alerts when creatinine rises –1.5× baseline — ensure medical team aware this has been generated. Medications list (full; include ALL OTC drugs).	AKI Stage 2 (creatinine 218; baseline 105). K+ 5.9 — ECG [result]. Haemodynamics: SBP 98; HR 108; temp 37.8; RR 20. Precipitants: ibuprofen OTC x4 days; lisinopril; furosemide; D&V x4 days. Background: CKD 3a; T2DM; hypertension. Drugs stopped at this consultation: ibuprofen (stopped; do not restart); lisinopril (stopped; restart plan post-recovery); furosemide (stopped); metformin (stopped; lactic acidosis risk). Possible sepsis source (CRP 42; WCC 11.2) — source not confirmed in primary care; blood cultures + IV antibiotics in hospital.
Nephrology — post-AKI follow-up (or if not recovering)	Post-AKI: routine at 4–6 weeks if recovering. Urgent if: Stage 3; glomerulonephritis; no recovery at 72 hours	Nephrology does not need to be involved in straightforward pre-renal AKI responding to IV fluids. Nephrology involvement triggers: Stage 3 AKI; AKI without clear cause; suspected glomerulonephritis (haematuria + red cell casts; proteinuria; systemic features); AKI not improving at 48–72 hours of treatment; AKI requiring RRT. GP follow-up post-AKI: creatinine at 4–6 weeks and 3 months; urine ACR; BP; medication reinstatement review; CKD stage re-evaluation.	For nephrology referral include: AKI episode details; recovery trajectory; baseline creatinine; CKD history; urine ACR (proteinuria); any haematuria; blood pressure; medication list pre-AKI; all changes made.
Urology — if post-renal obstruction identified	Same-day if obstruction causing AKI — hydronephrosis; anuria; retention	Not applicable to Mr. Patel unless bladder scan shows retention. For post-renal AKI: catheterise immediately (if in retention); renal USS (hydronephrosis = urology/nephrostomy); upper tract obstruction (bilateral = nephrostomy; unilateral in single kidney = urgent urology). Malignancy-related obstruction: oncology + urology.	USS results; catheter residual volume; suspected cause (stone; BPH; malignancy); creatinine trajectory.

🎓 SCA Checkpoint — Step 6TasksGlobal Skills

Referral to hospital

"I am calling the hospital now to arrange for you to go in today. I want to make sure you get there by ambulance — your blood pressure is lower than I am comfortable with and I do not want you driving or travelling by car. I will send with you a copy of your blood test results and a letter explaining exactly what is happening and what medicines I have stopped. Your wife is very welcome to come with you."

Deductions

Not arranging ambulance for a haemodynamically compromised patient — SBP 98 and patient being told to make their own way to hospital is a patient safety failure

Step 7

Management — STOP SADMAN · K+ Management · Fluid Status · SADMAN Education · Recovery Monitoring

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7A — Immediate actions in primary care (before and during hospital transfer)

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For Mr. Patel — five immediate actions while arranging hospital transfer

STOP ALL SADMAN DRUGS NOW — document in notes

Ibuprofen: STOP (never restart in CKD). Lisinopril: STOP (restart plan at 4–6 weeks post-recovery with monitoring). Furosemide: STOP (restart once haemodynamically stable and eGFR recovering). Metformin: STOP (restart when eGFR >30 and clinically well). Document: “Ibuprofen; lisinopril; furosemide; metformin all withheld at this consultation pending recovery. Amlodipine and atorvastatin continued.”

"I am stopping four of your medications today. They are all fine to take normally — but right now, with your kidneys under stress, they are making things worse. The hospital will tell you when to restart them."

ECG — K+ 5.9 requires cardiac monitoring

Perform ECG immediately. Look for: tall peaked T waves; PR prolongation; QRS widening. Any changes = 999 immediately + IV calcium gluconate if available. No changes: still urgent hospital (K+ can rise further without symptoms).

"I want to check your heart tracing right now — because with a high potassium level, we need to make sure your heart rhythm is not affected."

Arrange hospital admission by ambulance

Call medical registrar directly (or 999 if ECG changes). Haemodynamically compromised: ambulance essential. Provide: copies of blood results; ECG; drugs stopped; referral letter. Brief carer (wife): what to expect; which ward; what tests will happen.

"I am arranging an ambulance for you — your blood pressure is too low for you to travel safely by car."

Oral fluids while waiting if tolerating them

If patient can tolerate oral fluids and is not vomiting: encourage oral hydration while waiting for ambulance (small sips; 200–300 ml water; not fruit juice — avoid potassium-rich fluids in hyperkalaemia). Do not delay ambulance for this. If vomiting: no oral fluids; IV only in hospital.

"If you feel able to, sip some water slowly while you wait for the ambulance — but small sips only, and stop if you feel sick."

Brief SADMAN education before transfer — expand post-recovery

Mr. Patel needs to understand why ibuprofen was dangerous. A brief, non-blaming explanation now; full written SADMAN education at the post-AKI follow-up.

"The ibuprofen from the supermarket — it is a painkiller, but it reduces blood flow to the kidneys. For most people that is fine; but for you, with your kidney condition, and especially when you are dehydrated, it is one of the tablets you should never take without asking us first."

7B — Treatment goals

Acute treatment goals (hospital)

Restore renal perfusion — IV 0.9% NaCl; target urine output >0.5ml/kg/hCorrect hyperkalaemia — K+ <5.5 before discharge Treat sepsis source — blood cultures; IV antibiotics if pyelonephritisMonitor creatinine BD until recovering Creatinine returning towards baseline within 48–72 hoursBlood pressure stabilised; haemodynamics normal

GP follow-up goals (post-discharge)

Creatinine returned to baseline (or as close as possible) at 4–6 weeksACEi (lisinopril) safely restarted with monitoring Metformin restarted (eGFR >30 confirmed)CKD stage re-evaluated (may have progressed) SADMAN education completed; written information givenNSAIDs absolutely avoided; documented in notes Urine ACR checked post-AKI (proteinuria marker)Annual renal function monitoring established

7C — Non-medication management

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Fluid Management

IV 0.9% NaCl for dehydration; target 0.5ml/kg/h urine output; avoid overload

Hospital IV fluid management

Standard IV resuscitation: 0.9% NaCl (normal saline) in bolus doses (250–500ml over 15–20 minutes) until haemodynamics improve. After resuscitation: titrate IV fluid rate to urine output (target 0.5–1 ml/kg/hour). Monitor fluid balance carefully: in patients with CKD and cardiac risk (Mr. Patel), fluid overload is a real risk — target modest positive balance rather than aggressive resuscitation. Avoid: potassium-containing fluids (Hartmann’s contains 5 mmol/L K+ — use 0.9% NaCl in hyperkalaemia). Monitor Na+ (avoid hyponatraemia with large volumes of free water).

Oral advice (community AKI or post-hospital)

Maintain adequate oral hydration; 2–2.5 litres daily unless fluid-restricted. During illness: small; frequent oral fluids. If unable to maintain hydration orally (persistent vomiting): go to A&E. Avoid fruit juices; bananas; potatoes; tomatoes (high-potassium foods) while K+ is elevated.

IV fluid resuscitation restores renal perfusion in pre-renal AKI — first-line treatment

📐

SADMAN Sick-Day Rules Education

Written information; which drugs to hold; when to restart; when to seek help

SADMAN (Sick-Day Rules)

When to STOP (if vomiting; diarrhoea; reduced fluid intake; high fever; cannot eat or drink normally):
S — Sulphonylureas (gliclazide; glipizide — hypoglycaemia risk)
A — ACE inhibitors / ARBs (reduce GFR when dehydrated)
D — Diuretics (worsen volume depletion)
M — Metformin (lactic acidosis risk)
A — NSAIDs (nephrotoxic; reduce GFR)
N — NOACs/newer anticoagulants (accumulate in renal failure; bleed risk)

When to restart

Usually 24–48 hours after the patient is: eating and drinking normally; vomiting and diarrhoea resolved; feeling well. NOT at a fixed number of hours — when clinically recovered. Call GP surgery if uncertain. Seek urgent advice if: urine output drops significantly; signs of dehydration persist; potassium-related symptoms (palpitations; weakness; confusion).

SADMAN education is preventive: this AKI was preventable; written sick-day rules reduce recurrence

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Dietary Advice During AKI Recovery

Low-potassium diet until K+ normalised; adequate calories; avoid dehydration

During hyperkalaemia (K+ 5.5–6.5)

Avoid high-potassium foods: bananas; oranges; tomatoes; potatoes; spinach; avocado; nuts; dried fruit; dark chocolate; salt substitutes (often potassium chloride). Prefer: apples; pears; blueberries; white rice; white bread; pasta; vegetables (boiled in large volume water — leaches potassium). Adequate caloric intake important: malnutrition worsens AKI recovery and increases muscle breakdown (raises K+ from intracellular release). Referral to renal dietitian if hyperkalaemia is recurrent or severe.

Post-AKI fluid intake

2–2.5 litres daily (unless fluid-restricted for cardiac or other reasons). Maintain adequate hydration particularly in warm weather; exercise; illness. Report significant reduction in urine output (less than usual; darker than normal) to GP promptly.

Low-K+ diet during recovery reduces arrhythmia risk while kidneys clear excess potassium

💊

NSAIDs — Permanent Avoidance in CKD

NSAIDs contraindicated in CKD (eGFR <60); document; analgesia alternatives

Education and documentation

NSAIDs (ibuprofen; naproxen; diclofenac; aspirin at anti-inflammatory dose; COX-2 inhibitors) are contraindicated in CKD eGFR <60 and must be avoided. Add “NSAID — contraindicated CKD” to allergy/intolerance record in clinical system (not a true allergy; a contraindication — but flagging ensures pharmacy alert). Patient education: “Do not buy ibuprofen or naproxen from pharmacies or supermarkets — always check with us first.” Alternatives for musculoskeletal pain: paracetamol (1g QDS); topical diclofenac gel (local effect; minimal systemic absorption — NICE approved for localised musculoskeletal pain; lower nephrotoxicity risk; but use caution in severe CKD); codeine phosphate (opioid; constipation risk; dose reduction in CKD); physiotherapy.

The triple whammy

“Triple whammy” = NSAID + ACEi/ARB + diuretic: this specific combination carries the highest AKI risk. Document in notes: “NSAIDs contraindicated — triple whammy risk; CKD; previous AKI. Do not prescribe. Block on clinical system.”

NSAID contraindication documentation prevents recurrent AKI; a preventable patient safety event

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Post-AKI Monitoring Plan

Creatinine at 4–6 weeks; 3 months; annually; urine ACR; BP; medication review

Recovery monitoring

Creatinine at 4–6 weeks post-AKI: has it returned to baseline? If returned to baseline: restart ACEi (lisinopril); check K+ and creatinine 1–2 weeks later. Creatinine at 3 months: is the CKD stage changed? Urine ACR: check for proteinuria post-AKI (marker of ongoing tubular injury; indicates incomplete recovery or new CKD-related proteinuria). Blood pressure: may be difficult to manage with ACEi on hold — amlodipine (already on) provides bridge BP control.

Long-term

Annual renal function monitoring (CKD template or diabetic annual review). Annual urine ACR. BP target: <130/80 mmHg in CKD with diabetes. SADMAN reminder at every annual review. AKI recurrence risk: high — same precipitants can recur. Document: “AKI episode [date]; Stage 2; precipitants: ibuprofen; lisinopril; furosemide; D&V. SADMAN education given [date].”

Post-AKI monitoring reduces CKD progression; identifies incomplete recovery; guides medication reinstatement

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Medication Reinstatement Plan

Lisinopril at 4–6 weeks; metformin when eGFR >30; furosemide when stable; NSAIDs never

ACEi (lisinopril)

Restart at 4–6 weeks post-AKI once: eGFR returned to baseline (or close); patient clinically well; K+ <5.0 mmol/L. Check creatinine and K+ at 1–2 weeks after restarting. Long-term benefit (renal protection; BP; heart failure) outweighs the risk — it must be restarted. Document the plan explicitly in discharge summary and in the GP notes.

Metformin; furosemide; NSAIDs

Metformin: restart when eGFR >30 and clinically recovered. Monitor eGFR 1–2 weeks after restarting. Furosemide: restart once haemodynamically stable and eGFR recovering — may not need to restart at original dose if BP is better controlled without it. NSAIDs: DO NOT restart. Document as contraindicated. Add to clinical system alert. Alternative analgesia arranged.

Structured medication reinstatement prevents both under-prescribing (losing ACEi protection) and harm (premature ACEi restart before recovery)

7D — Prescribing guide

In the GP setting: the primary pharmacological intervention is NOT prescribing — it is STOPPING drugs. STOP ibuprofen; lisinopril; furosemide; metformin immediately and document. The hospital will manage IV fluids; hyperkalaemia treatment; and antibiotic choice if sepsis confirmed. GP prescribing role post-AKI: medication reinstatement plan; NSAID contraindication documented.

Immediate: STOP these drugs (all four for Mr. Patel)

Ibuprofen (OTC NSAID): STOP; do not restart; contraindicated in CKD; “triple whammy”; add contraindication to clinical record
Lisinopril (ACEi): STOP; restart at 4–6 weeks post-recovery with monitoring
Furosemide (diuretic): STOP; restart once haemodynamically stable and eGFR recovering
Metformin: STOP; restart when eGFR >30 and clinically recovered
Amlodipine and atorvastatin: continue — no dose adjustment needed in AKI

SADMAN drugs stopped: document explicitly in notes before hospital transfer.

Hyperkalaemia management — hospital-initiated

K+ 5.5–6.5 (no ECG changes): urgent hospital; stop K+-raising drugs; dietary K+ restriction; cardiac monitoring
K+ >6.5 or ECG changes: 999; IV calcium gluconate 10ml 10% (30ml over 10 min) immediately
Hospital: insulin/dextrose (10 units soluble insulin in 50ml 50% dextrose IV over 15–30 min); salbutamol 10–20mg nebulised; sodium bicarbonate if acidotic (pH <7.1)
Patiromer (Veltassa) or sodium zirconium cyclosilicate (Lokelma): oral K+ binders; used for chronic hyperkalaemia in CKD; can be used in hospital for acute management
Dialysis: if K+ unresponsive to medical treatment; anuric; severe metabolic acidosis

GP role: ECG; recognise urgency; communicate K+ clearly to receiving team. Do not attempt IV treatment without appropriate equipment and monitoring.

Post-AKI reinstatement (GP role; 4–6 weeks)

Lisinopril: restart once eGFR at or near baseline; K+ <5.0; patient well. Check creatinine and K+ 1–2 weeks after restarting.
Furosemide: restart with BP monitoring; may need dose review
Metformin: restart when eGFR >30 and clinically well; monitor eGFR 4–6 weeks after restarting
NSAIDs: NEVER restart; document contraindication permanently
Add “NSAIDs contraindicated — CKD; AKI [date]” to clinical record alert

ACEi must be restarted — renal protection long-term outweighs short-term AKI risk once recovered.

7E — Medication selector

Select AKI scenario for management guidance

STOP nephrotoxics (all AKI — first action) Stage 1 AKI; clinically stable; community management Stage 2–3 AKI; hospital admission (Mr. Patel) Hyperkalaemia K+ >5.5 — management Post-AKI recovery — medication reinstatement SADMAN sick-day rules education

AKI management guidance

ALL AKI — STOP NEPHROTOXICS first: ibuprofen/NSAIDs (STOP; contraindicated in CKD; do not restart); ACEi/ARBs (STOP; restart 4–6 weeks post-recovery); diuretics (STOP; restart when haemodynamically stable); metformin (STOP; restart when eGFR >30). Stage 1 stable: oral fluids; repeat bloods 24–48h; escalation criteria. Stage 2–3 / haemodynamically compromised (Mr. Patel): hospital admission by ambulance; ECG (K+ 5.9); IV 0.9% NaCl; K+ management; sepsis screen. K+ 5.5–6.5: urgent hospital; ECG; dietary K+ restriction; stop K+-retaining drugs. K+ >6.5 or ECG changes: 999; IV calcium gluconate; insulin/dextrose; salbutamol nebulised. Post-AKI: creatinine at 4–6 weeks and 3 months; urine ACR; BP; restart ACEi when near-baseline eGFR and K+ <5.0; check K+ and creatinine 1–2 weeks after restarting. NSAID contraindication documented permanently. SADMAN education: written leaflet; all SADMAN drugs identified; when to stop; when to seek help; when to restart.

7F — Drug reference cards

NSAIDs — STOP; Contraindicated in CKD

Ibuprofen · Naproxen · Diclofenac · COX-2 inhibitors · Triple whammy with ACEi + diuretic · Contraindicated eGFR <60

✗ STOP immediately — never restart in CKD or previous AKI; document contraindication permanently

STOP immediately — major AKI precipitant; do not restart in CKD or AKI historyNo dose — CONTRAINDICATED. Add to clinical system alert. Analgesia alternatives: paracetamol; topical NSAID; codeine

✗ Mechanism of nephrotoxicity

NSAIDs inhibit prostaglandin synthesis → constrict afferent arteriole → reduce glomerular filtration → AKI. Prostaglandins normally dilate the afferent arteriole to maintain GFR — blocking them in a patient who is dehydrated, on an ACEi, and on a diuretic removes the last compensatory mechanism maintaining renal perfusion. CONTRAINDICATED: eGFR <60 (CKD Stage 3–5); dehydration; cardiac failure; combination with ACEi + diuretic (“triple whammy”). Even topical NSAIDs have some systemic absorption — use cautiously in severe CKD. Add to allergy/contraindication record: “NSAIDs — contraindicated; CKD; AKI [date].”

✓ Analgesia alternatives for Mr. Patel

Paracetamol 1g QDS (max 4g/day; no dose reduction in CKD — preferred first-line analgesia in CKD). Topical diclofenac gel (Voltarol 12h Emulgel; local application; minimal systemic absorption; lower nephrotoxicity risk than oral NSAIDs; can use for localised musculoskeletal pain). Codeine phosphate 30mg QDS (opioid; dose reduction in CKD; constipation; sedation). Physiotherapy for back pain. Strong opioids (tramadol; morphine): use with great caution in CKD — accumulation of active metabolites; specialist advice. Lidocaine plasters (Versatis): neuropathic pain; minimal systemic absorption; safe in CKD.

💬 For Mr. Patel

"Ibuprofen is one of the main things that has caused this kidney problem. It reduces blood flow to the kidneys — and for you, with your kidney condition, that is dangerous. I am adding it to your record as something you should never take. For the back pain, paracetamol is safe and I will refer you to the physiotherapist."

NSAIDs: major AKI precipitant via afferent arteriole constriction; contraindicated eGFR <60; “triple whammy” with ACEi + diuretic. Document contraindication permanently. Alternative: paracetamol; topical NSAID (reduced systemic absorption); physiotherapy. SCA: not stopping ibuprofen in an AKI patient = patient safety fail; not identifying it as the precipitant = incomplete diagnosis.

ACE Inhibitors (Lisinopril) — Stop in AKI; Restart at 4–6 Weeks

Lisinopril · Ramipril · Enalapril · Perindopril · Stop in AKI — restart plan essential · Long-term renal protection

✗ STOP in AKI — restart plan essential; ACEi provides long-term renal protection in CKD + diabetes

STOP in AKI — withheld until eGFR near baseline; K+ <5.0; then restart with monitoringSTOP now. Restart lisinopril 5mg OD at 4–6 weeks — check K+ and creatinine 1–2 weeks after restarting

✗ Why stop in AKI

ACEi dilate the efferent arteriole → reduce glomerular hydrostatic pressure → GFR falls in states of low renal perfusion (dehydration; hypotension). In dehydration + NSAID + diuretic + ACEi — the “triple whammy” — GFR can drop precipitously. Must stop in AKI. Also hyperkalaemia risk increases in AKI when ACEi is continued. NEVER stop permanently without a restart plan — long-term ACEi in CKD with diabetes is evidence-based kidney protection (reduces progression to dialysis; reduces cardiovascular events; reduces albuminuria).

✓ Restart plan (mandatory)

Restart at 4–6 weeks post-AKI: confirm eGFR returned to baseline (or near); K+ <5.0 mmol/L; patient clinically well. Restart at the previous dose (lisinopril 5mg OD). Check U&Es at 1–2 weeks after restarting. If creatinine rises >30% from baseline on restarting: reduce dose; discuss with nephrology (this may indicate renal artery stenosis). If K+ rises above 5.5 after restarting: withhold; dietary advice; reassess. Document restart plan explicitly in notes and discharge summary.

🔬 Restart monitoring

U&Es and K+ before restarting (confirm near-baseline eGFR). U&Es at 1–2 weeks after restarting. Annual U&Es once stable. If K+ >5.5 on ACEi: consider potassium binder (patiromer; sodium zirconium cyclosilicate); dietary K+ restriction; check other K+-raising drugs (potassium-sparing diuretics; co-amoxiclav contains K+).

💬 Restart explanation

"The blood pressure tablet — lisinopril — I have stopped it for now because it reduces the blood flow to your kidneys when you are dehydrated. But it is actually very important for protecting your kidneys long-term with your diabetes, so I am going to restart it in about 4–6 weeks once your kidney function is back to normal. I will check blood tests before I do."

ACEi: stop in AKI (efferent dilation → reduces GFR in low-perfusion states). Restart plan mandatory (4–6 weeks; eGFR near baseline; K+ <5.0; monitoring after restart). Long-term kidney protection in CKD + diabetes — must be restarted. SCA: stopping without a restart plan = incomplete management; not documenting restart criteria = documentation failure.

Metformin — Stop in AKI; Lactic Acidosis Risk

Metformin 1g BD · Lactic acidosis if eGFR falls · Stop immediately in AKI · Restart when eGFR >30 · Reduce dose eGFR 30–45

✗ STOP in AKI — lactic acidosis risk; restart when eGFR >30 and clinically recovered

STOP immediately in AKI — accumulates; causes lactic acidosis; potentially fatalSTOP now. Restart metformin 1g BD when eGFR >30 and fully recovered; monitor eGFR 4–6 weeks after

✗ Lactic acidosis mechanism

Metformin is renally excreted. In AKI: metformin accumulates in plasma → inhibits mitochondrial complex I (oxidative phosphorylation) → forces anaerobic glycolysis → lactic acid accumulates → severe lactic acidosis (pH <7.1; lactate >5 mmol/L; mortality >50%). Lactic acidosis from metformin: encephalopathy; Kussmaul breathing; cardiovascular collapse; vomiting. Requires ICU; bicarbonate infusion; possible dialysis to clear metformin. Stop threshold: eGFR <30 (absolute); hold temporarily in any AKI episode. Do not restart until eGFR >30 and fully recovered from acute illness.

✓ Restart criteria

Restart when: eGFR >30; creatinine back to or near baseline; patient eating and drinking normally; no active acute illness. Check eGFR 4–6 weeks after restarting metformin. Reduce dose at eGFR 30–45 (metformin 500mg BD or 500mg TDS — maximum 1g/day at this eGFR). Contraindicated eGFR <30. If eGFR post-AKI does not return above 30: metformin cannot be restarted — alternative: gliclazide (dose carefully; hypoglycaemia risk); DPP-4 inhibitors (sitagliptin — renally dose-adjusted); SGLT-2 inhibitors (avoid if eGFR <45); insulin.

🔬 Monitor

Blood glucose during AKI hospital admission (may need insulin; sliding scale). eGFR at 4–6 weeks post-AKI before restarting. HbA1c at 3-month CKD/diabetes review — glycaemic control may have suffered during AKI.

💬 For Mr. Patel

"Your diabetes tablet — metformin — I am also stopping this for now. When the kidneys are struggling, metformin can build up in the blood and cause a serious problem with your blood chemistry. It is safe to restart once your kidneys have recovered — which I will check with a blood test in about 4–6 weeks."

Metformin: renally excreted; accumulates in AKI; causes lactic acidosis (pH <7.1; mortality >50%). Stop immediately in AKI. Restart when eGFR >30 and clinically recovered. eGFR 30–45: reduce dose. Contraindicated eGFR <30. SCA: not stopping metformin in AKI = serious patient safety failure.

Hyperkalaemia Management (K+ >5.5)

IV calcium gluconate · Insulin/dextrose · Salbutamol nebulised · Sodium bicarbonate · Patiromer (Veltassa) · Dialysis (severe)

🔴 K+ >6.5 or ECG changes = 999; IV calcium gluconate; insulin/dextrose; hospital emergency

Emergency if K+ >6.5 or ECG changes — 999; IV calcium gluconate first-line membrane stabiliserHospital only: IV calcium gluconate 10ml 10% over 2–5 min (ECG monitoring); insulin 10U soluble in 50ml 50% dextrose IV

✗ Emergency treatment sequence

K+ >6.5 or any ECG changes — 999 immediately. Hospital treatment: (1) IV calcium gluconate 10ml 10% over 2–5 min (under ECG monitoring) — membrane stabiliser; does NOT lower K+; prevents cardiac arrest while K+ is being lowered. (2) Insulin (10 units soluble) + 50ml 50% dextrose IV over 15–30 min — shifts K+ into cells; onset 15–30 min; lasts 4–6 hours. (3) Salbutamol 10–20mg nebulised — beta-2 agonist; shifts K+ into cells; onset 15–30 min. (4) Sodium bicarbonate 50–100 mmol IV if acidotic (pH <7.1). (5) Patiromer (Veltassa) or sodium zirconium cyclosilicate (Lokelma) oral — K+ binders; lower K+ over hours (not emergency drugs; adjuncts). (6) Haemodialysis if K+ unresponsive or anuric.

✓ GP role in hyperkalaemia

K+ 5.5–6.5 (no ECG changes): urgent hospital; ECG; stop all K+-raising drugs (ACEi; ARBs; potassium-sparing diuretics; trimethoprim; potassium supplements); low-K+ dietary advice; continuous K+ monitoring. K+ >6.5 or ECG changes: 999; if equipped: IV calcium gluconate in practice while awaiting ambulance (only if IV-trained and equipment available); do not delay 999 to attempt this in practice if not equipped.

🔬 Monitor after treatment

K+ every 2–4 hours until stable. ECG monitoring throughout. Once K+ <5.5 and stable: can de-escalate monitoring. Post-AKI: K+ returns to normal as kidneys recover. K+ persistently elevated (>5.5 mmol/L) despite AKI resolution: suspect Addison’s disease; renal tubular acidosis type 4; investigate; nephrology opinion.

💬 Mr. Patel — K+ 5.9 explanation

"Your potassium is a bit higher than it should be. Potassium is a chemical that your kidneys normally filter out — when the kidneys are under stress, it can build up. At the level yours is now, it is not immediately dangerous, but it needs monitoring and treatment in hospital because if it goes higher it can affect your heart rhythm."

Hyperkalaemia management: K+ 5.5–6.5 = urgent hospital + ECG + stop K+-raising drugs; K+ >6.5 or ECG changes = 999 + IV calcium gluconate (membrane stabiliser — does NOT lower K+). Hospital: insulin/dextrose; salbutamol; sodium bicarbonate if acidotic; patiromer/Lokelma; dialysis if severe. SCA: recognising K+ 5.9 as urgent (not normal; not simply monitoring); arranging ECG and hospital admission = Tasks marks.

Diuretics (Furosemide) — Stop in AKI; Restart When Stable

Furosemide 40mg · Spironolactone · Bendroflumethiazide · Stop in pre-renal AKI — worsens volume depletion · Restart with monitoring

✗ STOP in pre-renal AKI — worsens dehydration; restart when haemodynamically stable and eGFR recovering

STOP in pre-renal AKI — worsens volume depletion; restart when stableSTOP furosemide 40mg now. Restart when haemodynamically stable and eGFR recovering; may need dose review

✗ Why stop in pre-renal AKI

Loop diuretics (furosemide; bumetanide) cause natriuresis and water loss → volume depletion → worsens pre-renal AKI. In a patient already dehydrated from D&V, furosemide accelerates the problem. Spironolactone and amiloride: additionally cause hyperkalaemia — must stop in AKI when K+ is already elevated. Thiazides (bendroflumethiazide): also worsen volume depletion; often ineffective at eGFR <30. EXCEPTION: in fluid-overloaded AKI (cardiac failure; nephrotic syndrome), diuretics may be needed — specialist decision.

✓ Restart criteria

Restart furosemide when: haemodynamically stable; eGFR returning towards baseline; no longer oliguric; BP controlled. May need to restart at a lower dose if underlying volume status has changed. Review indication: does Mr. Patel still need furosemide? If no signs of fluid overload and BP controlled with amlodipine — furosemide may not need to be restarted at all; reassess clinical need.

💬 For Mr. Patel

"The water tablet — furosemide — I am also stopping that. It makes your body get rid of more water, which is exactly the wrong thing when you are already dried out from the sickness and diarrhoea. Once you have recovered, we can reassess whether you still need it."

Furosemide: worsens pre-renal AKI via volume depletion. Stop immediately. Restart when haemodynamically stable and eGFR recovering. Review clinical need post-AKI — may not need to restart at same dose. Exception: fluid-overloaded AKI (cardiac failure) — diuretics may be needed (specialist). SCA: stopping furosemide as part of complete SADMAN drug stop = Tasks mark.

SADMAN Sick-Day Rules — Patient Education

S — Sulphonylureas · A — ACEi/ARBs · D — Diuretics · M — Metformin · A — NSAIDs · N — NOACs · Written information; when to stop; when to restart

✓ Preventive education — provide written SADMAN rules at post-AKI review; this AKI was preventable

All patients on SADMAN drugs — annual sick-day rules education; written leaflet; in clinical notesNon-pharmacological education: written leaflet; verbal explanation; documented in notes

✓ SADMAN — full mnemonic for patient education

When to TEMPORARILY STOP if acutely unwell (vomiting; diarrhoea; unable to drink normally; fever; sweating profusely):
S — Sulphonylureas (gliclazide; glipizide; glimepiride): risk of hypoglycaemia when not eating — stop temporarily; resume when eating normally
A — ACE inhibitors/ARBs (lisinopril; ramipril; losartan; candesartan): reduce GFR in dehydration — stop temporarily
D — Diuretics (furosemide; spironolactone; bendroflumethiazide): worsen dehydration — stop temporarily
M — Metformin: lactic acidosis risk if kidneys struggling — stop temporarily
A — NSAIDs (ibuprofen; naproxen; diclofenac): reduce kidney blood flow — NEVER take if feeling unwell with CKD (consider permanent contraindication)
N — NOACs/newer anticoagulants (apixaban; rivaroxaban; edoxaban): accumulate in renal failure; haemorrhage risk — stop temporarily; warfarin: INR may become erratic during illness — check INR; seek advice
When to restart: 24–48 hours after eating and drinking normally; vomiting/diarrhoea resolved. Contact GP if not sure. SEEK URGENT HELP if: significantly reduced urine output; persistent vomiting >48 hours; feeling very unwell; palpitations or weakness.

✗ Delivery and documentation

Written SADMAN leaflet must be provided: THINK KIDNEYS (thinkigneys.org.uk) provides NHS sick-day rules leaflets for patients. Document in clinical notes: “SADMAN sick-day rules provided verbally and in writing [date].” Provide at: every annual CKD review; every annual diabetes review; every blood pressure review; at hospital discharge post-AKI. This is a preventive safeguarding measure — Mr. Patel’s AKI was preventable with prior SADMAN education.

💬 For Mr. Patel at post-AKI review

"I want to give you some important information about what to do with your tablets if you are ever unwell again — like when you had the sickness and diarrhoea. Some of your tablets are fine to take normally but become dangerous when you are dehydrated. Here is a card that lists them: the A — your blood pressure tablet; the D — the water tablet; the M — the metformin; and the A — the ibuprofen you bought. If you are ever vomiting or have diarrhoea or cannot eat or drink properly — stop these tablets until you are back to normal. If you are unsure — call us."

SADMAN education: preventive; this AKI was caused by failure to stop NSAID + ACEi + diuretic in dehydrated patient. Provide written leaflet; document provision. Not a prescribing action — an educational action. SCA: mentioning SADMAN sick-day rules and arranging written information at post-AKI review demonstrates understanding of primary prevention; Tasks and Relating to Others marks.

7G — Psychosocial context of AKI

🧑️

AKI in the context of Mr. Patel’s life — 72 years old; CKD; diabetes; carer is his wife; fear of dialysis; fear of hospital

AKI is a frightening diagnosis for a patient with CKD and diabetes who knows his kidneys are not perfect. The fear of dialysis; the disruption of a hospital admission; and the confusion about why so many familiar tablets have been suddenly stopped all need to be addressed directly and compassionately.

💕

Fear of Dialysis

Every patient with CKD fears AKI means starting dialysis. Be specific and honest: “This kind of kidney injury — from dehydration and the tablets — usually recovers well with treatment. Dialysis is for kidney failure that does not recover — that is not where you are right now. We are catching this early enough to make a real difference.”

"I want to reassure you — this type of kidney injury, found early, almost always recovers. You are not looking at dialysis from this episode."

🧑️

Involving the Carer

Mr. Patel’s wife called this morning — she is the informant and the carer. Include her explicitly in the management discussion (with Mr. Patel’s consent). She needs to understand: why he is going to hospital; what to expect; when to call 999 while waiting for the ambulance. SADMAN education must also be given to the carer.

"I want to make sure your wife is part of this conversation — she called this morning because she was concerned, and she needs to know what to do while you wait for the ambulance and what to expect at the hospital."

💊

Medication Stopping — Anxiety

Patients are often anxious when multiple familiar tablets are stopped suddenly. They may fear their blood pressure; diabetes; or heart condition will deteriorate. Explain each stopping decision specifically and the restart plan: “These tablets are all going to be restarted once your kidneys have recovered — none of them are being stopped permanently.” Exception: ibuprofen — that IS being stopped permanently.

"I am stopping four tablets today — but I want to reassure you that three of them will be restarted once you have recovered. Only the ibuprofen is being stopped permanently."

🔋

Non-Blame for Ibuprofen

Mr. Patel bought ibuprofen over the counter — he did not know it was dangerous for him. The explanation must be non-blaming: “The ibuprofen was a completely understandable thing to reach for with a bad back — you could not have known it would cause this. The important thing is that we know now, and we can prevent it from ever happening again.”

"I want to be clear — you did not do anything wrong by taking ibuprofen for your back. You did not know it could be harmful for your kidneys. That is something we should have explained more clearly before."

📈

Realistic Prognosis

Pre-renal AKI from a clear cause (dehydration; drug-induced), caught early: expected recovery to baseline or near-baseline. The honest message: “Most people with the kind of kidney injury you have recover to where they were before. There is a small chance your kidney baseline may end up slightly lower after this — but with the right treatment and the right medicines afterwards, we give your kidneys the best chance.”

"The likely outcome — with treatment starting today — is that your kidneys recover back to where they were. I want to be honest that there is a small chance they may be slightly lower afterwards, but that is the exception, not the rule, when we catch it early."

📹

This AKI Was Preventable

Mr. Patel’s AKI was caused by a combination that could have been avoided with sick-day rules knowledge. The post-AKI SADMAN education is a safeguarding action — not a criticism of the patient. Document as a significant event: AKI Stage 2 in a patient with CKD; consider significant event review; SADMAN education as preventive action for the future.

"After you have recovered, I want to make sure this never happens again. I am going to give you a card that lists which tablets to stop if you are ever sick or vomiting in the future."

7H — Follow-up

Today — STOP SADMAN; ECG; hospital admission by ambulance

STOP: ibuprofen; lisinopril; furosemide; metformin. Continue: amlodipine; atorvastatin. ECG performed (K+ 5.9). Urine dip + MSU. Hospital arranged by ambulance (haemodynamically compromised). Carer briefed. Blood test results and referral letter with patient. Brief SADMAN education given. Full written SADMAN at post-discharge GP review.

Hospital admission today — non-negotiable

Post-discharge GP review — 1–2 weeks

Hospital discharge summary received? Bloods post-discharge: creatinine; eGFR; K+; Na+. Is eGFR recovering? Furosemide: restart if haemodynamically indicated and eGFR recovering. Metformin: not yet (eGFR needs to be >30 and stable). Lisinopril: not yet (4–6 weeks). BP: amlodipine providing cover. Full SADMAN education: written leaflet provided; carer present if possible. NSAIDs: permanently contraindicated — document in system.

Creatinine; K+; eGFR; discharge summary; SADMAN written information

4–6 weeks — ACEi reinstatement review

Creatinine and eGFR: returned to baseline (or near)? K+ <5.0? Clinically well? If yes: restart lisinopril 5mg OD. Check U&Es at 1–2 weeks after restarting lisinopril. Metformin: restart if eGFR >30 and stable (check dose — may need reduction at eGFR 30–45). Urine ACR: proteinuria post-AKI? CKD stage reassessment: has it progressed? Analgesia plan for back pain (paracetamol; physio; no NSAIDs).

Lisinopril restart decision; metformin restart; urine ACR; CKD stage

3 months — CKD stage confirmation; HbA1c; cardiovascular risk

Creatinine and eGFR at 3 months: has eGFR stabilised at or near pre-AKI baseline? If eGFR lower than pre-AKI: CKD stage upgrade (may have moved from 3a to 3b or 4). Urine ACR: persistent proteinuria = CKD progression marker; nephrology referral if new or worsening proteinuria. HbA1c (glycaemic control may have suffered during admission). BP. Medication check: all SADMAN drugs at appropriate doses with eGFR at 3 months.

CKD stage; urine ACR; HbA1c; BP; medication review at 3-month eGFR

Annually — CKD + diabetes review; SADMAN re-education

Annual renal function monitoring (U&Es; eGFR; urine ACR; BP). SADMAN re-education: “reminder — you had a serious kidney episode last year; here are the tablets to stop if you become unwell.” NSAIDs: re-confirm as permanently contraindicated. AKI recurrence risk: document in notes and share with out-of-hours and community teams. If eGFR declining: nephrology referral (eGFR <30 or rapid decline).

Annual renal; SADMAN reminder; NSAIDs never; nephrology if eGFR declining

7I — Monitoring — CLUE mnemonic

CLUE monitoring mnemonic for AKI

Creatinine/eGFR: staged; tracked; returned to baseline? Lisopril (ACEi)/K+: restart plan; K+ <5.0 before restart; check 1–2 weeks after. Urine ACR: proteinuria post-AKI = marker of renal injury; CKD stage. Education: SADMAN sick-day rules written; documented; re-given annually.

Parameter	Monitor	Timing	Action
Creatinine / eGFR	Recovery to baseline? CKD stage post-AKI?	At discharge; 4–6 weeks; 3 months; annually	Not recovering at 72 hours: nephrology. New CKD stage upgrade: additional proteinuria monitoring; nephrology if eGFR <30.
Potassium	AKI hyperkalaemia resolving? Before ACEi restart	With each creatinine check; before ACEi restart	K+ persistently >5.5 despite recovery: Addison’s; RTA type 4; nephrology. K+ <5.0 before restarting ACEi.
Urine ACR	Proteinuria post-AKI; tubular injury marker	4–6 weeks post-AKI; annually	New proteinuria: CKD progression; nephrology referral if ACR >70 mg/mmol new post-AKI.
SADMAN drugs	All correctly managed; restart plan enacted	4–6 weeks (restart); 3 months; annually	NSAIDs: never restart. ACEi: restart 4–6 weeks with monitoring. Metformin: restart eGFR >30.

Milestone	Action
Post-discharge 1–2 weeks	Creatinine; K+; SADMAN written info; discharge summary reviewed
4–6 weeks	ACEi restart; metformin restart if eGFR >30; urine ACR; CKD stage
3 months	CKD stage confirmed; HbA1c; BP; full medication review at current eGFR
Annually	CKD + diabetes review; SADMAN re-education; NSAIDs never; nephrology if declining

7J — Safety-netting

⚠ Three critical safety-nets

Documentation requirements

AKI Stage 2 documented: creatinine 218 vs baseline 105 = 2.08× — NICE CG169 criteria met

All four SADMAN drugs documented as stopped at this consultation with rationale and restart plan

ECG performed and result documented (K+ 5.9 — ECG changes or no changes)

Hospital admission arranged; ambulance; referral letter and blood results sent with patient

NSAIDs permanently contraindicated — added to clinical system alert; “ibuprofen: CKD; AKI; contraindicated”

SADMAN education: verbal and written; documented; plan for 4–6 week creatinine and ACEi restart review

999 (while waiting)Palpitations; collapse; confusion; anuria — do not wait for arranged ambulance

1–2 weeksPost-discharge bloods; SADMAN written; discharge summary reviewed

4–6 weeksACEi restart decision; metformin restart; urine ACR; CKD stage

🎓 SCA Checkpoint — Step 7 (Final)TasksRelating to OthersGlobal Skills

Closing the consultation

"Let me pull together what is happening. Your kidneys have been under significant stress — four things hit them at once: the sickness and diarrhoea dehydrating you; the ibuprofen reducing blood flow to your kidneys; your blood pressure tablet; and your water tablet. All four made things worse together."

"I am stopping four of your tablets today — the ibuprofen; the blood pressure tablet; the water tablet; and the metformin. Three of those will be restarted once you have recovered. The ibuprofen should never be taken again."

"I have arranged an ambulance to take you to hospital today. Before you go: I want to make sure your wife knows that if you develop a fast or irregular heartbeat; feel faint; or stop passing urine completely — call 999 immediately."

"When you come out of hospital — book a blood test with us in 4–6 weeks. Don’t restart the blood pressure tablet or the metformin until I have told you it is safe. Is there anything you want me to explain again before the ambulance comes?"

Deductions

Not identifying ibuprofen (OTC) as a precipitant — the most important and preventable cause
Not stopping metformin — lactic acidosis risk is a serious patient safety failure
Not performing ECG with K+ 5.9 — cardiac arrhythmia could be imminent
Attempting community management of Stage 2 AKI with K+ 5.9 + haemodynamic compromise
Not providing a restart plan for ACEi — stopping without restart plan = incomplete management

Tasks summary

AKI Stage 2 (2.08× baseline) staged correctly
All four SADMAN drugs stopped (ibuprofen; lisinopril; furosemide; metformin)
ECG performed (K+ 5.9)
Hospital admission by ambulance arranged
ACEi restart plan (4–6 weeks)
NSAIDs permanently contraindicated; SADMAN education

Relating to Others

“Triple whammy” explained in plain language
Fear of dialysis addressed specifically and honestly
Non-blame for ibuprofen use
Carer briefed; 999 criteria explained
Medication stopping anxiety addressed

🔴 Red

Ibuprofen not identified; metformin not stopped; ECG not performed; hospital not arranged; K+ 5.9 not acted upon; no restart plan; community management of Stage 2 AKI with haemodynamic compromise

🟠 Amber

Ibuprofen identified and stopped; lisinopril stopped; hospital arranged; ECG performed; furosemide and metformin not stopped; no restart plan for ACEi; SADMAN not explained; NSAIDs not documented as permanently contraindicated

🟩 Green

All four SADMAN drugs stopped (ibuprofen; lisinopril; furosemide; metformin); AKI Stage 2 staged; ECG performed; hospital admission by ambulance; K+ 5.9 communicated to receiving team; triple whammy explained; fear of dialysis addressed; 4–6 week ACEi restart plan; NSAIDs permanently contraindicated; SADMAN education verbal + written plan; carer briefed; 999 criteria; closing question

"My wife called this morning because I’ve been really unwell for 4 days — diarrhoea and vomiting. I’ve been taking ibuprofen for my back pain because I couldn’t take paracetamol [incorrect belief — paracetamol is safe]. I feel exhausted and I haven’t passed much urine today."

Who you are

Derek Patel, 72, retired engineer. Type 2 diabetes (well-controlled; HbA1c 48); hypertension; CKD Stage 3a (eGFR 52; creatinine 105 six weeks ago). Metformin 1g BD; lisinopril 5mg OD; furosemide 40mg OD; amlodipine 5mg OD; atorvastatin 40mg OD. Self-medicating ibuprofen 400mg TDS for 4 days (bought from supermarket for a bad back). 4 days D&V. Lethargic; oliguria today. Wife phoned surgery.

Hidden agenda — disclose if GP creates space

Fear of dialysis (disclose if asked about concerns): “My brother had kidney problems and ended up on dialysis. Am I going to end up like that?”

Hospital reluctance: “I really don’t want to go to hospital — can we not sort this out here?” — Respond well if GP explains specific reasons (potassium; IV fluids) in plain language.

Paracetamol misconception: “I thought I couldn’t take paracetamol — someone told me it was bad for kidneys.” — This is a misconception; paracetamol is safe in CKD; the GP should correct this gently.

Responses to key conversations

When ibuprofen raised: Surprised: “I had no idea ibuprofen could do that — it’s just a painkiller you can buy in a supermarket.”
Non-blame acknowledgement: “Oh — so this is not my fault?” — Respond with relief if GP is explicit that ibuprofen is freely sold and the patient was not warned adequately.
On stopping all the tablets: Anxious: “But I need my blood pressure tablets — what happens to my blood pressure if I stop them?” — Respond well to: “Amlodipine will still be keeping your blood pressure under control; it is only the lisinopril we are stopping temporarily.”
Challenge: “I looked online and it said AKI can cause permanent kidney damage — is my CKD going to get much worse from this?”

Clinical details

BP 98/62; HR 108; temp 37.8°C; RR 20; O2 sat 97%
Dry mucous membranes; reduced skin turgor; low JVP — dehydrated
Loin tenderness bilateral (mild) — may indicate pyelonephritis contribution
No bladder palpable (oliguria; not retention)
GCS 15; alert; orientated; worried

"I looked online and it said AKI can cause permanent kidney damage — is my CKD going to get much worse? Am I going to end up on dialysis like my brother?"

Ideal GP response: “The honest answer is: AKI from dehydration and medications, caught at this stage, most commonly recovers back to baseline. There is a small chance your kidneys may be a little lower afterwards — but that is the exception, not the rule. Dialysis is for kidney failure that does not recover — that is not where you are right now. We are catching this early enough to make a real difference.” Mr. Patel: “OK — if going to hospital is going to help my kidneys recover, I’ll go. Can my wife come?”

🏥

Clinic Quick Reference

AKI — Clinical Decision Framework

NICE CG169 · STOP SADMAN · AKI Stage 1–3 · K+ emergencies · ECG mandatory K+ >5.5 · Community vs hospital · Recovery monitoring · ACEi restart plan

▼expand

💊 1 — AKI Triage and Action

AKI suspected → Stage (creatinine vs baseline) → STOP SADMAN → K+ management → Admit vs community → Recovery plan

🔴 999 / Emergency

K+ >6.5 or ECG changes → 999; IV calcium gluconate
qSOFA ≥2 (septic shock) → 999; Sepsis 6
Stage 3 AKI; anuria; pulmonary oedema; encephalopathy

999 / Same-day emergency admission

🟠 Urgent Hospital (Mr. Patel)

Stage 2 AKI + K+ 5.9 + haemodynamic compromise + CKD
Stage 1 not responding; or K+ 5.5–6.5; or severe comorbidity
Unable to maintain oral hydration; persistent vomiting

Same-day ambulance; STOP SADMAN; ECG; referral letter

🟩 Community (Stage 1)

Stage 1; normotensive; drinking; K+ <5.5; no systemic illness
Clear pre-renal cause; likely to improve with oral fluids

STOP SADMAN; oral fluids; repeat bloods 24–48h; escalation criteria

📊 2 — Key Clinical Numbers

STOP SADMAN — first action

S — Sulphonylureas; A — ACEi/ARBs; D — Diuretics; M — Metformin; A — NSAIDs; N — NOACs. STOP immediately in any AKI; document each with restart plan.

K+ >6.5 = 999

Any K+ >6.5 or ECG changes: 999; IV calcium gluconate (membrane stabiliser — does NOT lower K+). K+ 5.5–6.5: ECG; urgent hospital.

AKI Stage 2 = 2.0–2.9× baseline

Stage 1: 1.5–1.9×. Stage 2: 2.0–2.9×. Stage 3: ≥3.0× or ≥354 µmol/L. Always use baseline (most recent 3–12 months).

Triple whammy: NSAID + ACEi + diuretic

Highest-risk polypharmacy combination for AKI. Any patient on all three: SADMAN education mandatory; NSAID contraindicated in CKD.

Metformin: lactic acidosis

Stop in AKI. Accumulates → blocks mitochondrial oxidative phosphorylation → lactic acidosis (mortality >50%). Restart when eGFR >30.

ACEi: restart 4–6 weeks

Stop in AKI; restart when eGFR near baseline; K+ <5.0. Check U&Es 1–2 weeks after. Must be restarted — long-term kidney protection.

NSAIDs: contraindicated eGFR <60

Permanent contraindication in CKD Stage 3–5 and post-AKI. Document in clinical system alert. Alternative: paracetamol; topical NSAID; physiotherapy.

Pre-renal: 70% of community AKI

Volume depletion most common. IV 0.9% NaCl first-line in hospital. Avoid if fluid overloaded (cardiac failure) — specialist decision.

ECG mandatory: K+ >5.5

Peaked T waves (earliest sign) → PR prolongation → QRS widening → sine wave → VF. Any change = 999 + IV calcium gluconate.

AKI 1-year mortality: 20–25%

Significant long-term risk of CKD; cardiovascular events; recurrent AKI. Post-AKI monitoring plan is not optional.

Urine ACR post-AKI

Proteinuria post-AKI = marker of ongoing tubular injury or CKD progression. Check at 4–6 weeks and annually.

SADMAN education

Written sick-day rules at every annual CKD/diabetes review; at hospital discharge post-AKI. Think Kidneys leaflet (thinkidneys.org.uk). Document provision.

⚠ 3 — CLUE Monitoring

CLUE	Parameter	Timing	Action
Creatinine/eGFR	Recovery to baseline? CKD stage change?	4–6 weeks; 3 months; annually	Not recovering at 72h: nephrology. CKD stage upgrade: nephrology if eGFR <30.
Lisinopril/K+	ACEi restart criteria met? K+ <5.0?	4–6 weeks; 1–2 weeks after restart	K+ <5.0 and near-baseline eGFR: restart. Check U&Es 1–2 weeks after.
Urine ACR	Proteinuria post-AKI?	4–6 weeks; annually	New proteinuria: CKD progression; nephrology if ACR >70 mg/mmol.
Education	SADMAN written; NSAIDs contraindicated; documented	Post-discharge; annually	Not given: provide at 4–6 week review; document. Re-give at every annual CKD/diabetes review.

🎓

SCA Exam Quick Reference

AKI SCA — STOP SADMAN · AKI Stage 2 (2.08×) · ECG K+ 5.9 · Hospital by ambulance · Triple whammy · ACEi restart plan · NSAIDs never · SADMAN education

NICE CG169 · Mr. Patel: ibuprofen + lisinopril + furosemide + D&V · K+ 5.9 · CKD 3a · Metformin lactic acidosis · CLUE monitoring

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💬 Opening & ICE

Opener: “I can see from your blood tests that your kidneys are under significant stress. Tell me about the diarrhoea and vomiting — when did it start; how much have you been able to drink; and has your urine been less than usual?”

OTC drugs: “Have you taken any painkillers recently — including anything you bought yourself from a pharmacy or supermarket?”

ICE — Ideas: Triple whammy explained in plain language: “Four things hit your kidneys at once — the diarrhoea; the ibuprofen; the blood pressure tablet; the water tablet.”

ICE — Concerns: Dialysis fear: “This type of AKI, caught at this stage, almost always recovers. Dialysis is for kidney failure that does not recover — that is not where you are.”

ICE — Expectations: Hospital: “Two specific reasons you need hospital: the potassium needs cardiac monitoring; you need IV fluids faster than drinking can provide.”

Non-blame: “You could not have known the ibuprofen was dangerous for you — this is something we should have explained before.”

✅ Key SCA Tasks (15pt)

All 4 SADMAN drugs stopped (2pt): Ibuprofen (STOP; never restart; contraindicated in CKD). Lisinopril (STOP; restart 4–6 weeks). Furosemide (STOP; restart when stable). Metformin (STOP; lactic acidosis; restart eGFR >30). Amlodipine + atorvastatin: continue. Each documented with rationale and restart criteria.

AKI staged (2pt): Creatinine 218 ÷ baseline 105 = 2.08× = Stage 2. Staging requires baseline creatinine. Stage 2 + K+ 5.9 + haemodynamic compromise = hospital.

K+ 5.9 + ECG (2pt): ECG mandatory (peaked T waves; PR prolongation). No changes: urgent hospital. Changes: 999 + IV calcium gluconate. K+ communicated to receiving team.

Hospital by ambulance (2pt): SBP 98 = haemodynamically compromised; ambulance essential. Referral letter + bloods + ECG + stopped drug list. Carer briefed on 999 criteria while waiting.

SADMAN education + NSAIDs permanently contraindicated (2pt): Verbal today; written leaflet at 4–6 week review. Clinical system alert: “NSAIDs contraindicated — CKD; AKI [date].” Document provision.

Metformin lactic acidosis (1pt): Stopped immediately; specific explanation; restart criteria (eGFR >30; clinically recovered).

Post-AKI monitoring (1pt): Creatinine at 4–6 weeks; urine ACR; ACEi restart criteria (near-baseline eGFR; K+ <5.0; check U&Es 1–2 weeks after).

Sepsis features assessed (1pt): qSOFA; NEWS2; infection source; MSU; hospital team briefed re IV antibiotics if pyelonephritis.

Obstruction excluded (1pt): Urine output (oliguria not anuria); no palpable bladder; documented as considered.

Analgesia alternative (1pt): Paracetamol 1g QDS (safe in CKD); physiotherapy; NSAIDs never again.

🔴 Not stopping metformin = serious safety failure

🔴 No ECG with K+ 5.9 = patient safety failure

🔴 Community management of Stage 2 + K+ 5.9 + SBP 98 = clinical fail

👥 Relating to Others (11pt)

Urgency without panic (1pt): “Significant stress — prompt treatment makes a real difference”

ICE: Ideas — triple whammy (1pt): Four simultaneous causes; accessible language

ICE: Concerns — dialysis fear specific (1pt): “Not where you are; caught early”

ICE: Expectations — hospital specific reasons (1pt): Potassium monitoring + IV fluids — two reasons

Non-blame for ibuprofen (1pt): “Sold in supermarkets; you could not have known”

Drug stopping anxiety addressed (1pt): “Three will be restarted; only ibuprofen permanently off”

Carer briefed; 999 criteria (1pt): Palpitations; collapse; anuria — call 999; do not wait

Prognosis honest + specific (1pt): “Most recover to baseline; small chance of lower baseline”

SADMAN empowering (1pt): “So this never happens again; card for the future”

What to expect in hospital (1pt): “IV fluids; cardiac monitoring; kidney checks every few hours”

Closing question — carer included (1pt): Both patient and wife asked; genuine pause

💊 Management Quick-Pick

Acute Kidney Injury · GP Clinical Reasoning Framework v2 · NICE CG169 (2013; updated 2020): Acute kidney injury · KDIGO AKI Clinical Practice Guideline 2012 (Kidney Disease: Improving Global Outcomes) · NICE CKS: AKI (2024) · Think Kidneys: sick-day rules and patient education resources (thinkidneys.org.uk) · NG133 (2019) Common mental health problems — not applicable here · Joint Formulary Committee: BNF for prescribing in renal impairment · MHRA: metformin and renal impairment guidance (2022)

Teaching clinicians why each step matters — not just what to do · Always consult current NICE CG169; KDIGO; and BNF · Clinical judgement takes precedence over any framework

Acute Kidney Injury

Red Flags — requiring 999 / same-day hospital admission

Safeguarding — AKI in Older Adults and Polypharmacy

💊 Medication safety

🧑️ Capacity and carer involvement

🚘 Community vs hospital decision

📸 Sick-day rules education

Immediate Life-Threatening

Same-Day Hospital (Not 999 Yet)

AKI Stage 1; Clinically Well

Intrinsic AKI (ATN; GN)

Pyelonephritis-precipitated AKI

STOP ALL SADMAN DRUGS NOW — document in notes

ECG — K+ 5.9 requires cardiac monitoring

Arrange hospital admission by ambulance

Oral fluids while waiting if tolerating them

Brief SADMAN education before transfer — expand post-recovery

Select AKI scenario for management guidance

Fear of Dialysis

Involving the Carer

Medication Stopping — Anxiety

Non-Blame for Ibuprofen

Realistic Prognosis

This AKI Was Preventable

Today — STOP SADMAN; ECG; hospital admission by ambulance

Post-discharge GP review — 1–2 weeks

4–6 weeks — ACEi reinstatement review

3 months — CKD stage confirmation; HbA1c; cardiovascular risk

Annually — CKD + diabetes review; SADMAN re-education

CLUE monitoring mnemonic for AKI

⚠ Three critical safety-nets

Documentation requirements

🎭 Patient actor brief — Mr. Derek Patel, 72

Who you are

Hidden agenda — disclose if GP creates space

Responses to key conversations

Clinical details